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Defective Decidualization During and After Severe Preeclampsia Reveals a Possible Maternal Contribution to the Etiology

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Defective Decidualization During and After Severe Preeclampsia Reveals a Possible Maternal Contribution to the Etiology Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology Tamara Garrido-Gomeza,b,c,d, Francisco Dominguezb, Alicia Quiñonerob, Patricia Diaz-Gimenob, Mirhan Kapidzicc,d, Matthew Gormleyc,d, Katherine Onac,d, Pablo Padilla-Isertee, Michael McMasterf, Olga Genbacevc,d, Alfredo Peralese,g, Susan J. Fisherc,d,h,i,1,2, and Carlos Simóna,b,g,j,1,2 aFundación Igenomix, 46980 Valencia, Spain; bInstituto Universitario IVI, Instituto de Investigación Sanitaria Hospital Clinico de Valencia INCLIVA, 46010 Valencia, Spain; cCenter for Reproductive Sciences, University of California, San Francisco, CA 94143; dDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, CA 94143; eDepartment of Obstetrics and Gynecology, Hospital Universitario La Fe, 46026 Valencia, Spain; fDepartment of Cell and Tissue Biology, University of California, San Francisco, CA 94143; gDepartment of Obstetrics and Gynecology, School of Medicine, Valencia University, 46010 Valencia, Spain; hThe Eli & Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, CA 94143; iDepartment of Anatomy, University of California, San Francisco, CA 94143; and jDepartment of Obstetrics and Gynecology, School of Medicine, Stanford University, Palo Alto, CA 94305 Edited by R. Michael Roberts, University of Missouri-Columbia, Columbia, MO, and approved August 11, 2017 (received for review April 20, 2017) In preeclampsia (PE), cytotrophoblast (CTB) invasion of the uterus in studying the CTB subpopulation that invades the uterine wall in and spiral arteries is often shallow. Thus, the placenta’s role has the context of this syndrome. Targeted analyses of particular mo- been a focus. In this study, we tested the hypothesis that decidual lecular families, such as the vascular-type adhesion molecules that defects are an important determinant of the placental phenotype. are up-regulated as the extravillous CTBs enter the uterine wall, We isolated human endometrial stromal cells from nonpregnant revealed focal defects in differentiation (8). These results were donors with a previous pregnancy that was complicated by severe confirmed and augmented by global transcriptional profiling of PE (sPE). Compared with control cells, they failed to decidualize in CTBs isolated from the placentas of affected pregnancies as they vitro as demonstrated by morphological criteria and the analysis of differentiated along the invasive pathway over a period of 48 h in stage-specific antigens (i.e., IGFBP1, PRL). These results were bol- culture (9). The surprising finding that the abnormal pattern of stered by global transcriptional profiling data that showed they gene expression autocorrected to control levels by the end of the were transcriptionally inert. Additionally, we used laser microdissec- culture period pointed to a potentially important role for paracrine tion to isolate the decidua from tissue sections of the maternal–fetal effectors. In this regard, the decidua, which supports placental interface in sPE. Global transcriptional profiling revealed defects in growth and function, is a prime candidate. gene expression. Also, decidual cells from patients with sPE, which In humans, formation of the decidua does not depend on the dedifferentiated in vitro, failed to redecidualize in culture. Condi- presence of a conceptus (10). This progressive process, which tioned medium from these cells failed to support CTB invasion. To mimic involves hormonally regulated differentiation of human endo- aspects of the uterine environment in normal pregnancy, we added metrial stromal cells (hESCs), begins during the midsecretory PRL and IGFBP1, which enhanced invasion. These data suggested that phase of the menstrual cycle (11). The transformation is initiated failed decidualization is an important contributor to down-regulated in areas that are immediately adjacent to the uterine spiral ar- CTB invasion in sPE. Future studies will be aimed at determining teries, ultimately spreading throughout the entire endometrium whether this discovery has translational potential with regard to (12). In vivo and in vitro, this process is driven by increasing levels – assessing a woman’s risk of developing this pregnancy complication. of progesterone and local cAMP production (13 15), which preeclampsia | human endometrial stromal cells | decidua | Significance cytotrophoblast | transcriptomics We provide evidence of a decidualization defect in the endo- reeclampsia (PE), which affects ∼8% of first-time pregnan- metrium of women with severe preeclampsia (PE) that was Pcies, impacts 8 million mother–infant pairs worldwide each detected at the time of delivery and persisted years after the year (1, 2). This complication, which is specific to human preg- affected pregnancy. We went on to link this defect to impaired nancy, is characterized by the new onset of hypertension, pro- cytotrophoblast invasion. The transcriptional signature of the teinuria, and other signs of maternal vascular damage such as defect could enable its detection before (or after) conception, edema (3). Severe PE (sPE) is diagnosed based on a further ele- which would aid the development of therapies focused on vation of blood pressure (systolic pressure ≥160 mm Hg or diastolic improving decidualization and perhaps preventing severe PE. pressure ≥110 mm Hg) or any of the following: thrombocytopenia, impaired liver function, progressive renal insufficiency, pulmonary Author contributions: O.G., A.P., S.J.F., and C.S. designed research; T.G.-G., F.D., A.Q., M.K., K.O., P.P.-I., O.G., and A.P. performed research; P.D.-G. and M.G. contributed new edema, and the new onset of cerebral or visual disturbances (4). reagents/analytic tools; T.G.-G., M.G., S.J.F., and C.S. analyzed data; P.P.-I. collected samples; Currently, the only definitive cure is delivery of the placenta and and T.G.-G., M.M., S.J.F., and C.S. wrote the paper. therefore the infant. As a result, PE accounts for 15% of preterm The authors declare no conflict of interest. births in the United States. Despite decades of research, a full This article is a PNAS Direct Submission. understanding of PE pathogenesis remains elusive, which com- Freely available online through the PNAS open access option. pounds the difficulties involved in the identification of predictive Data deposition: The data reported in this paper have been deposited in the Gene Ex- biomarkers and the development of targeted therapeutic strategies. pression Omnibus (GEO) database, https://www.ncbi.nlm.nih.gov/geo (accession nos. It is widely believed that the placenta plays a central role, with GSM2420587–GSM2480236). deficient cytotrophoblast (CTB) invasion of uterine spiral arte- 1S.J.F. and C.S. contributed equally to this work. rioles being a casual factor (5, 6). Currently, the pathogenesis of 2To whom correspondence may be addressed. Email: [email protected] or PE is conceptualized in a two-stage model, with the placental [email protected]. defect precipitating an abnormal maternal response that manifests This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10. as the signs (7). Accordingly, there has been a great deal of interest 1073/pnas.1706546114/-/DCSupplemental. E8468–E8477 | PNAS | Published online September 18, 2017 www.pnas.org/cgi/doi/10.1073/pnas.1706546114 Downloaded by guest on October 1, 2021 stimulate the synthesis of a complex network of intracellular and finding suggested that in vitro decidualization was impaired in PNAS PLUS secreted proteins that regulate decidualization (16). hESCs obtained from patients with former sPE compared with Morphologically, this process is characterized by the transforma- controls. tion of elongated fibroblast-like cells into an enlarged polygonal- or round-shaped population, a process that involves complex cyto- Alterations in the Global Transcriptional Profiles of Decidualized skeletal rearrangements (17). Actin, which is concentrated in the hESCs from Patients with Former sPE. Next, we used a microarray cortex of decidual cells, most often in a filamentous form (i.e., strategy to identify the molecular changes underlying the functional F-actin), regulates the intracellular reorganization and resulting decidualization defect found in hESCs from women who had ex- shape changes (18–20). Decidualization can also be viewed as a perienced sPE. Specifically, we carried out a transcriptomic analysis process whereby the cells acquire a secretory phenotype. Decid- of hESCs that were established from the normal pregnancy and sPE ualized hESCs secrete specific products such as prolactin (PRL) groups described earlier, nondecidualized and decidualized in vitro and insulin-like growth factor binding protein 1 (IGFBP1). Thus, (Fig. 2A). The clinical characteristics of the endometrial donors these proteins have been widely used as markers of decidualized are shown in SI Appendix,TableS2. An overview of the results is cells (21). They also play an important role in endometrial differ- presentedinFig.2B. In the nondecidualized state, only five statis- entiation and control of CTB invasion (22, 23). Overall deciduali- tically significant genes were differentially expressed between the zation helps regulate embryo implantation, and subsequently, CTB control and the sPE samples, and the fold differences were modest interactions with the uterus, making this process an essential com- (Fig. 2C). Thus,
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